This proposal aims to understand the mechanism by which Wnt5A controls metastatic behavior in melanoma. The first aim will identify the Wnt5A receptor relevant to melanoma. It is my hypothesis that the relevant Wnt5A receptor is differentially expressed in different stages of melanoma cells. The second specific aim will identify the relevant pathway that Wnt5A signals through. It is my hypothesis that Wnt5A induces metastatic behavior in melanoma through one of the three known Wnt signaling pathways. The third Aim will identify potentially novel signaling components involved in metastatic behavior in melanoma using functional proteomics to profile changes in the melanoma proteome and phosphoproteome in response to Wnt5A.